aldh1a2 polyclonal antibody rabbit (Thermo Fisher)
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Aldh1a2 Polyclonal Antibody Rabbit, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/aldh1a2+polyclonal+antibody+rabbit/pmc09025022-128-29-34
Average 90 stars, based on 1 article reviews
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1) Product Images from "Inhibition of RhoA and Cdc42 by miR-133a Modulates Retinoic Acid Signalling during Early Development of Posterior Cardiac Tube Segment"
Article Title: Inhibition of RhoA and Cdc42 by miR-133a Modulates Retinoic Acid Signalling during Early Development of Posterior Cardiac Tube Segment
Journal: International Journal of Molecular Sciences
doi: 10.3390/ijms23084179
Figure Legend Snippet: Whole-mount ISH for miR-133a and whole mount IMH for RhoA, Cdc42 and Raldh2 during early chick cardiac development, from HH8–HH11 stages, in control embryos. Note miR-133a expression pattern at the level of the anterior region of the primitive endocardial tube (PET), being observable in the atrium (A) and ventricle (V) at later stages. Note the location of RhoA, Cdc42 and Raldh2 at the level of the PET posterior region, and subsequently in the atrium and inflow tract (IFT). The scheme illustrates the complementary location in cranial-caudal trend of miR-133a (blue) in comparison with RhoA, Cdc42 and Raldh2 (orange).
Techniques Used: Expressing
Figure Legend Snippet: Effect of miR-133a gain- and loss-of-function on posterior cardiac segment. Whole-mount IMH for RhoA, Cdc42 and Raldh2. and ISH for Tbx5 and AMHC1. Embryos microinjected with CFDA (control), premiR-133a or antimiR-133a, at the level of the posterior cardiac precursors of both primitive endocardial tubes, and visualisation of CFDA ( A ). Note that, at the atrium and inflow tract levels, RhoA ( B ), Cdc42 ( C ), Raldh2 ( D ), Tbx5 ( E ) and AMHC1 ( F ) are dramatically reduced, and an atrophic sino-atrial region in the heart tube after premiR-133a treatment is indicated by the red arrows, whereas they are markedly increased and expanded after miR-133a inhibition (blue arrows). RT-qPCR of RNA from dissected cardiac asa (left side) in embryos microinjected either with CFDA, premiR-133a or antimiR-133a. A high level of miR-133a leads to decreased RhoA, Cdc42, Raldh2, Tbx5 and AMHC1 transcripts, whereas miR-133a inhibition leads to increased transcripts. The standard deviations are from three independent experiments. Student’s t -test: * p < 0.05, ** p < 0.01, *** p < 0.005 with respect to control (CFDA) embryos.
Techniques Used: Inhibition, Quantitative RT-PCR
Figure Legend Snippet: Whole-mount ISH for miR-133a, Tbx5 , AMHC1 and IMH for Raldh2. Embryos microinjected with CFDA (control), Retinoic acid (RA) or Citral, at the level of the posterior cardiac precursors into both primitive endocardial tubes, and visualisation of CFDA ( A ). The gain-of-function of RA leads to diminished miR-133a expression (red arrows) at the cardiac asa level ( B ), accompanied by increased protein levels of Raldh2 ( C ) and expanded expression of Tbx5 ( D ) and AMHC1 ( E ) in the heart tube and in the inflow tract (blue arrows). Note atrophic sino-atrial region with increased miR-133a expression (blue arrows) at cardiac asa level ( B ), and also (red arrows) diminished Raldh2 protein level ( C ), and decreased Tbx5 ( D ) and AMHC1 ( E ) expressions by RA synthesis inhibition. RT-qPCR of RNA from dissected cardiac asa (left side) in embryos microinjected either with CFDA, RA or Citral. The standard deviations are from three independent experiments. Student’s t -test: * p < 0.05, ** p < 0.01, *** p < 0.005 with respect to control (CFDA) embryos.
Techniques Used: Expressing, Inhibition, Quantitative RT-PCR
Figure Legend Snippet: Model proposed for the interplay between miR-133a and RA during posterior heart tube formation. Our model indicates that miR-133a downregulates RhoA and Cdc42. Consequently, Raldh2 downregulation is induced by miR-133a, via these Rho GTPases. RA synthesis is Raldh2-dependent. Thus, miR-133a modulates RA signalling via Raldh2 expression. Also, RA negatively modulates miR-133a expression during the early genetic programme of the sinoatrial region. Additionally, our model indicates that miR-133a modulates cell proliferation by acting on the cell cycle regulators p21 (via RhoA) and cyclin A (via Cdc42). We hypothesise that there is a negative feedback mechanism between miR-133a and RA signalling during early development of the posterior cardiac tube segment. A: anterior segment, P: posterior segment.
Techniques Used: Expressing
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Control:Article Title: Inhibition of RhoA and Cdc42 by miR-133a Modulates Retinoic Acid Signalling during Early Development of Posterior Cardiac Tube Segment Article Snippet: .. Experimental and control (CFDA) embryos were subjected to whole mount IMH was performed as previously described by us [ , ], using RhoA Polyclonal Antibody Rabbit (1:300, Invitrogen, OSR00266W), |




